Researchers are investigating a number of theories to explain how clinical depression affects the body. A leading area of research focuses on the levels of certain chemicals in the brain that regulate mood, especially the neurotransmitters norephinephrine and serotonin. People with depression may have reduced levels of these neurotransmitters, or be unable to properly utilize them. Currently, drug therapy for depression focuses on boosting levels of these mood-enhancing neurotransmitters, especially serotonin.

Another idea from Duke University Medical Center is that depression interferes with the body’s natural baroreflex sensitivity (BRS). When functioning properly, BRS helps the body to adjust to the common changes in blood pressure that occur throughout the day. For example, pressure rises when the heart increases its pumping activity. This causes arteries to dilate and special nerve receptors to stretch. The stretching of these receptors then signals the heart to decrease pumping activity so pressure will not get too high. Without properly adjusting to changes in blood pressure, the heart is working harder and is more at risk of heart disease.

A reduction in BRS has been found to occur in people diagnosed with clinical depression, as well as in people who have experienced a heart attack or who have been diagnosed with an abnormal heart rhythm (arrhythmia). Moreover, reduced BRS can be a harbinger of future life-threatening arrhythmias, such as ventricular tachycardia.

A third theory is based on the finding that clinically depressed people have higher levels of stress hormones (e.g., adrenaline and cortisol) than do people without clinical depression, and their sympathetic nervous system, which controls the “fight or flight” response, is activated. This may help explain why the hearts of clinically depressed people beat faster, even during sleep. It is also consistent with studies showing that people with both heart disease and clinical depression have reduced heart rate variability – the heart’s ability to handle stress.

Frequent or consistently high levels of stress hormones have also been linked to:

• Certain types of chest pain (angina) and abnormal heart rhythms 
  
  
• Increased risk of blood clots and high blood pressure (hypertension)
  
  
• Cardiac ischemia (a condition in which the heart does not get enough blood)
  
  
• Higher cholesterol and higher risk of hardening of the arteries (atherosclerosis)
  
  
• Reduced effectiveness of some heart medications

Another theory is that depressed heart patients are less likely to exercise, spend time with family and friends, participate in rehabilitation, or follow their medication plans. They may also be more likely to “self-medicate” their depression by smoking, drinking alcohol or eating unhealthy “comfort foods.” Because they are more likely to experience chest pain, the pain may also further their isolation and inactivity.

Although studies have established links between depression and heart disease, much more research must be done to reveal the actual mechanism behind this link. For instance, researchers discovered that it is possible to predict the risk of depression by measuring the severity of atherosclerosis. However, they do not know if atherosclerosis causes depression or whether both conditions are symptoms of some other underlying process.